Telomeres and Female Reproductive Aging

Kalmbach, Keri; Antunes, Danielle Mota Fontes; Kohlrausch, Fabiana B.; Keefe, David L.

doi:10.1055/s-0035-1567823

Cited by 34 publications

(16 citation statements)

References 81 publications

(89 reference statements)

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“…Reducing oxidative stress by supplementation of melatonin could potentially reduce mitochondrial ROS-induced damage, thus maintaining the number and quality of oocytes and follicles. Telomere shortening is considered as a biomarker of cellular senescence and is highly sensitive to oxidative stress 34 35 . Telomere dysfunction may contribute to reproductive aging-associated meiotic defects, miscarriage and infertility 36 .…”

Section: Discussionmentioning

confidence: 99%

Melatonin improves age-induced fertility decline and attenuates ovarian mitochondrial oxidative stress in mice

Song

Peng

Yin

et al. 2016

Sci Rep

110

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Increasing evidence shows that melatonin protected against age-related mitochondrial oxidative damage. However, the protective effects of melatonin against ovarian aging has not been explored. Young Kunming females (aged 2–3 months) were fed with melatonin added to drinking water for 6 or 12 months (mo). We found that long-term (12 mo) melatonin treatment significantly reduced ovarian aging, as indicated by substantial increases in litter size, pool of follicles, and telomere length as well as oocyte quantity and quality. Melatonin treatment suppressed ovarian mitochondrial oxidative damage by decreasing mitochondrial reactive oxygen species (mROS) generation, inhibiting apoptosis, repressing collapse of mitochondrial membrane potential and preserving respiratory chain complex activities. Female mice fed with melatonin had enhanced mitochondrial antioxidant activities, thus reducing the risk of mitochondrial oxidative damage cause by free radicals. Notably, melatonin treatment enhanced SIRT3 activity but not the protein expression level, and increased the binding affinity of FoxO3a to the promoters of both superoxide dismutase 2 (SOD2) and catalase (CAT). In conclusion, melatonin exerted protection against aging-induced fertility decline and maintenance of mitochondrial redox balance.

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Section: Discussionmentioning

confidence: 99%

Melatonin improves age-induced fertility decline and attenuates ovarian mitochondrial oxidative stress in mice

Song

Peng

Yin

et al. 2016

Sci Rep

110

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“…Several potential molecular mechanisms contribute to ovarian aging, including metabolic/energetic disorders, telomere shortening (Kalmbach et al 2015), impaired DNA repair (Titus et al 2015) and mitochondrial dysfunction (Wang et al 2017). Mitochondria are the cellular energy producers and are the most abundant organelles within oocytes.…”

Section: Introductionmentioning

confidence: 99%

Evidence that growth hormone can improve mitochondrial function in oocytes from aged mice

Hou

Wang

et al. 2019

Reproduction

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Decline in successful conception decreases more rapidly after 38 years of age owing to follicular depletion and decreased oocyte quality. However, limited information is available regarding the underlying mechanism and the useful treatment. This study aimed to evaluate the effects of growth hormone supplementation on oocyte maturation in vivo in aged and young mice and to determine its effect on mitochondrial function. The influence of three different doses of recombinant human growth hormone (rhGH) (0.4, 0.8 and 1.6 mg/kg/day) for 8 weeks before ovarian stimulation was analyzed. Superovulated oocytes were released from the oviduct of 12-week-old and 40-week-old female C57BL/6J mice 14–16 h after administration of human chorionic gonadotropin. Ovarian follicle and morphological analysis and oocyte maturation parameters were then evaluated. This study is the first, to our knowledge, to report that medium- and high-dose rhGH significantly increases antral follicles in aged mice but anti-Müllerian hormone (AMH) levels. Furthermore, derived oocytes, MII-stage oocyte rate, ATP levels, mitochondrial membrane potential and frequencies of homogeneous mitochondrial distribution increased. In contrast, in both aged and young mice, the mtDNA copy numbers per oocyte were similar before rhGH administration, and upon saline administration, they did not differ significantly. We conclude that medium-dose rhGH supplementation before standard ovarian stimulation regimens improves oocyte quality in aged mice, probably by enhancing mitochondrial functionality.

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“…4 Patients who present with ovarian aging are commonly di- There are several potential molecular mechanisms contributing to ovarian aging, including impaired DNA repair, 6 telomere shortening, 7 metabolic/energetic disorders, and mitochondrial dysfunction.…”

Section: 3mentioning

confidence: 99%

Mitochondrial dysfunction and ovarian aging

Wang

Zhang

Jiang

et al. 2017

American J Rep Immunol

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Mitochondria are double‐membrane‐bound organelles that are responsible for the generation of most of the cell's energy. Mitochondrial dysfunction has been implicated in cellular senescence in general and ovarian aging in particular. Recent studies exploited this association by studying mitochondrial DNA (mtDNA) copy number as a potential biomarker of embryo viability and the use of mitochondrial nutrients and autologous mitochondrial transfer as a potential treatment for poor ovarian function and response.

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Telomeres and Female Reproductive Aging

Cited by 34 publications

References 81 publications

Melatonin improves age-induced fertility decline and attenuates ovarian mitochondrial oxidative stress in mice

Melatonin improves age-induced fertility decline and attenuates ovarian mitochondrial oxidative stress in mice

Evidence that growth hormone can improve mitochondrial function in oocytes from aged mice

Mitochondrial dysfunction and ovarian aging

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